The molecular mechanisms through which ghrelin exerts its cardioprotective effects during cardiac remodeling post-myocardial infarction (MI) are poorly understood. The aim of this study was to investigate whether the cardioprotection mechanisms are mediated by modulation of JAK/STAT signaling and what triggers this modulation. Rats were divided into six groups (n = 12/group): control, sham, sham + ghrelin (100 µg/kg, s.c., daily, starting 1 day post-MI), MI, MI+ ghrelin, and MI+ ghrelin+ AG490, a potent JAK2 inhibitor (5 mg/kg, i.p., daily). All treatments were administered for 3 weeks. Administration of ghrelin to MI rats improved left ventricle (LV) architecture and restored cardiac contraction. In remote non-infarcted areas of MI rats, ghrelin reduced cardiac inflammation and lipid peroxidation and enhanced antioxidant enzymatic activity. In addition, independent of the growth factor/insulin growth factor-1 (GF/IGF-1) axis, ghrelin significantly increased the phosphorylation of JAK2 and Tyr702 and Ser727 residues of STAT3 and inhibited the phosphorylation of JAK1 and Tyr701 and Ser727 residues of STAT1, simultaneously increasing the expression of BCL-2 and decreasing in the expression of BAX, cleaved CASP3, and FAS. This effect coincided with decreased expression of SOCS3. All these beneficial effects of ghrelin, except its inhibitory action on IL-6 expression, were partially and significantly abolished by the co-administration of AG490. In conclusion, the cardioprotective effect of ghrelin against MI-induced LV injury is exerted via activation of JAK2/STAT3 signaling and inhibition of STAT1 signaling. These effects were independent of the GF/IGF-1 axis and could be partially mediated via inhibition of cardiac IL-6.

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Problem statement:Cadmium is one of the most dangerous occupational and environmental toxins. It is found in drinking water, atmospheric air and even in food. Cadmium is reported to be very toxic to biological systems. Until now in treating intoxication with this metal, chelating Compounds have been used, burdened with numerous undesirable symptoms. For this reason, many researches are carried out in many countries to find natural-made compounds that help in the protection against cadmium induced toxicity with fewer or no side effects. This study was conducted to demonstrate the effect of daily oral Camel's milk administration against Cadmium chloride induced toxicity in white albino rats. Approach: White albino rats of both sexes (230-250 g) were housed in standard metal cages (6 rats/cage). The experimental rats (6 in each group) distributed into two experimental groups with a shared control group received only normal saline orally (Group 1). In experimental first group a daily dose (10 mg kg  1 body weight) of cadmium chloride was orally administrated to the rats for 21 days and named Cadmium chloride treated rats. In experimental second group, the same concentrations of cadmium chloride was dissolved in 2 mL of early morning fresh Camel's milk and the whole solution was administered into the experimental rats for 21 days and named Camel's milk cadmium chloride treated group. Water and food were provided ad libitum. Results: The data indicated that, in experimental Cadmium chloride treated rats, serum albumin, calcium and blood hemoglobin were decreased compared with control group received normal saline only. Moreover, Camel's milk administration with cadmium chloride showed a significant improvement of albumin, hemoglobin and calcium levels in the serum of the rats compared with cadmium chloride treated rats. Serum iron, sodium, chloride and urea levels were significantly increased in cadmium chloride treated rats compared with control group, while the addition of camel's milk to cadmium chloride decreased the high levels of these serum parameters in the treated rats. The enzyme activities of serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and serum Alkaline Phaospatase (ALP) were significantly increased by orally administration of cadmium chloride compared with control group, while adding Camel's milk to cadmium chloride decreased the high levels of these enzymes comparing with the cadmium chloride treated rats. Cadmium chloride administration resulted in a high concentration of lipid peroxidation markers; TBARS and Hydroperoxides in comparison to control group, adding camel's milk to the cadmium chloride restored the levels of these markers to their normal levels in comparing to Cadmium chloride treated rats. Also treatment with cadmium chloride alone caused a significant decrease in both the enzymatic and nonenzymatic markers of oxidative stress (superoxide dismutase and catalase) and reduced glutathione, respectively in the liver tissues of treated rats, while the admini...

Aim: To investigate the possible role of oxidative stress as a common mediator of apoptosis and cardiac damage in diabetes. Materials and Methods:This experimental work was conducted on 5 groups of Wistar rats. Group I was the control group. Diabetes type 1 was induced in other groups (by streptozotocin) and animals received insulin or vitamin E (300 mg /kg body weight), both insulin and vitamin E, or no treatment for 4 weeks according to their group. At the end of the study, serum and cardiac tissues were examined for biochemical parameters of cardiac function, oxidative stress and apoptosis. Electron microscopy pictures of cardiac tissue were also evaluated for signs of cardiac damage.Results: Markers of oxidative stress, apoptosis, inflammation as well as manifestations of cardiac damage as assessed by electron microscopy were significantly decreased in rats treated with both insulin and vitamin E when compared with untreated diabetic rats or rats treated with either insulin or vitamin E alone.Conclusion: Administration of both vitamin E and insulin was effective in reducing markers of oxidative stress and apoptosis and improving parameters of cardiac function in experiments animals. Antioxidants might prove beneficial as an adjuvant treatment in addition to insulin in type 1 diabetes associated with manifestations of cardiac complications.

Problem statement: Cadmium is a heavy metal of wide occupational and environmental contamination. In recent years, however, Cadmium has been implicated in the pathogenesis of several clinical disorders. One of the most frequently described problems in aluminum toxicity is anemia. Therefore, the present study was carried out to determine the effectiveness of Camel's milk in alleviating the toxicity of Aluminum Chloride (AlCl 3 ) on certain hematological parameters and antioxidant system components in the RBC's of white albino rats. Approach: Albino rats of both sexes (6/group) weighting between 230-250 g were divided into three treatment groups: Group one were rats given normal saline and served as control group, group two were rats treated with 2 mL of a solution containing cadmium chloride (10 mg kg −1 ) and named Cadmium chloride treated rats, group 3 were rat treated with 2 mL of a solution containing Camel's milk in which the same concentration of cadmium chloride was dissolved and named Camel's milk and Cadmium chloride treated rats. Rats were orally administered their respective doses every day for 21 days. Evaluations were made for hematological parameters in the blood and for oxidative stress components in the RBC's. Results: Results obtained showed that oral Cadmium chloride treatment caused a significant decrease in total red blood cell counts, Hematocrite (PCV) value, Hemoglobin (Hb) concentration, Meancorpuscular Volume (MVC), Mean Hemoglobin Concentration (MHC) and Mean Corpuscular Hemoglobin Concentration (MCHC). Also oral administration of Cadmium chloride induced free radicals and as a result caused a significant decrease in the activities of Superoxide Dismutase (SOD), Catalsae (CAT) and reduced glutathione (SGH) in the RBCs homolysate. The oral administration of Camel's milk with cadmium chloride alleviated it's toxic effect. Camel's milk administration resulted in a significant increase in the in total erythrocytes count, blood Hb, PCV, MCV, MHC and MCHC. Camel's milk reduced free radicals production and oxidative stress status in the RBC's noticed by the significant increased activities of SOD and CAT, as well as concentrations reduced glutathione (SGH). Conclusion: The above results indicated a protective effect of camel's milk oral administration against cadmium induced anemia and oxidative stress in the RBC's of white albino rats.

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Khat chewing is a recreational habit known to pose major socio-economic and medical problems in countries of Southern Arabia and the Horn of Africa. Among other adverse health effects, khat chewing has been associated with an increased risk of myocardial infarction (MI) in heavy consumers. This study was carried out to examine the direct effects of Catha edulis extract on contractility of spontaneously contracting, isolated rabbit heart and to investigate its mechanism of action. Isolated six rabbit's hearts attached to a Langendorff apparatus were perfused with extract at a constant flow rate and continuously bubbled with a 95% O2/5% CO2 gas mixture. Each heart served as its own control, as responses were recorded before and after administration of C. edulis extract. Varying concentrations of extract (50, 100 and 250 mg/ml) were loaded in the perfusate, their effects recorded and effluent fluid collected for assay of cardiac enzymes. Histological examination of the cardiac tissue was performed at the end of perfusion with 250 mg/ml extract. This study revealed that acute exposure to C. edulis extract exerted negative inotropic and chronotropic effects on isolated hearts. The extract also had a vasoconstrictor effect on coronary vessels, independent of α1 adrenergic receptor stimulation. Histological examination of hearts perfused with 250 mg/ml C. edulis extract revealed the presence of histological changes unique to myocardial infarction, a finding consistent with observed increased levels of cardiac enzymes in perfusates. Thus, we have demonstrated experimentally a direct cardiac depressant- and MI inducing effects of C. edulis extract. These results are consistent with the earlier reported deleterious effects of khat on cardiovascular function among khat chewers.